Berberine Attenuated Oxidative Stress Induced by Sodium Nitrite in Rat Liver

Abstract

Background: Berberine is a well-known alkaloid derived from Berberis species. Objectives: The present study aimed to investigate the hepatoprotective properties of berberine and elucidate its probable mechanisms against sodium nitrite toxicity. Methods: Forty animals were randomly classified into five equal groups to be treated for 60 days, including group 1: Control, group 2: Berberine-treated (100 mg/kg), group 3: Sodium nitrite-treated (80 mg/kg), group 4: Sodium nitrite together with 50 mg/kg of berberine, and group 5: Sodium nitrite together with 100 mg/kg of berberine. The protective effects of berberine against sodium nitrite induced-liver damage were investigated using parameters related to oxidative stress, inflammation, fibrosis, and apoptosis in the hepatocytes. Results: Treatment of rats with sodium nitrite considerably increased alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities, malondialdehyde (MDA) content, tumor necrosis factor (TNF)-α expression, caspase-3 activity, and transforming growth factor (TGF)-β1 concentration (P < 0.05) and significantly declined the levels of reduced glutathione (GSH), glutathione reductase (GR), glutathione S-transferase (GST), and glutathione peroxidase (GPx) (P < 0.05). The treatment of intoxicated rats with 100 mg/kg of berberine significantly reversed these changes and reached the values approximately to the normal level. However, berberine 50 mg/kg failed to normalize the disturbances. Conclusions: This study demonstrated that berberine could decrease sodium nitrite-induced liver injury in a dose-dependent manner probably due to its antioxidant, anti-inflammatory, anti-apoptotic, and antifibrotic capacities.